The Effect Of Cyclophosphamide On Sendai Virus Infection Of Mice

Robinson, T. W. E.; Cureton, R. J. R.; Heath, R. B.

doi:10.1099/00222615-2-2-137

Cited by 41 publications

(29 citation statements)

References 1 publication

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“…The Cy treatment of animal hosts infected with various viruses appeared to result in two categories of consequences according to the host-parasite relationships : (1) infections and resulting diseases are potentiated by suppressed immune responses [1,6,7,20,22,24,25,27,29,42,45,46], and (2) infections are either potentiated or not influenced but the disease manifestations are suppressed by depression of the immunopathological mechanisms leading to produce lesions [5, 10-12, 31,33]. In both cases, concerning viral infections, many reports described the occurrence of immunosuppression of humoral antibody responses, while in several [12] relevance of cell-mediated immune response was suggested from experimental data.…”

Section: And Methodsmentioning

confidence: 99%

Intestinal Resistance in the Experimental Enteric Infection of Mice with a Mouse Adenovirus

Hashimoto

Okada

Tajiri

et al. 1973

Japanese Journal of Microbiology

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The influence of cyclophosphamide (Cy) on the establishment and duration of the intestinal resistance against enteric infection with a mouse adenovirus, strain K87, was examined in inbred mice, strain DK1. When Cy (40 mg/kg/day) was administered to mice for 17 days from the time of virus challenge, a clear prolongation of viral growth and a delayed appearance of neutralizing (NT) antibody in the intestinal wall as well as in the serum were observed. When Cy (40 mg/kg/day, for 14 days) was administered after cessation of viral growth (4 to 6 weeks after virus challenge) and part of the mice were rechallenged with the virus, titers of NT antibody and immunoglobulins became significantly lower than those in control mice not treated with Cy, and regrowth of the virus was observed in eight out of twenty-five Cy-treated mice, regardless of the presence or absence of rechallenge. In this experiment, antibody titers in the intestinal contents of eight virus-positive mice were significantly lower than those of the remaining seventeen virus-negative mice. The time when the decrease of intestinal NT antibody was maximum coincided with the time of the maximal frequency of viral regrowth. It was discussed that these facts might present an evidence to support the idea that the intestinal resistance was acquired through local NT antibody belonging to-IgA in the intestinal tract.

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Section: And Methodsmentioning

confidence: 99%

Intestinal Resistance in the Experimental Enteric Infection of Mice with a Mouse Adenovirus

Hashimoto

Okada

Tajiri

et al. 1973

Japanese Journal of Microbiology

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“…Mice immunosuppressed with Cvtoxan and infected intranasally with Sendai virus develop higher titers of virus in the lung and have more extensive histologic lesions than nonimmunosuppressed control mice (19). In experiments in which intranasal infection of mice with Sendai virus was potentiated by immunosuppression, serum antibody titers were found to be suppressed (19). This does not prove, however, that this suppression of antibody formation resulted in the increased severity of this infec-tion.…”

Section: Discussionmentioning

confidence: 69%

“…Exceptions to this general observation sometimes occur when experimental respiratory and intracranial viral infections are studied. Mice immunosuppressed with Cvtoxan and infected intranasally with Sendai virus develop higher titers of virus in the lung and have more extensive histologic lesions than nonimmunosuppressed control mice (19). In experiments in which intranasal infection of mice with Sendai virus was potentiated by immunosuppression, serum antibody titers were found to be suppressed (19).…”

Section: Discussionmentioning

confidence: 84%

“…In recent years it has been demonstrated that an immune response is critical in recovery from a number of experimental, primary viral infections (4)(5)(6)(7)(17)(18)(19)(20)(21). There are a number of possible mechanisms by which the immune response might contribute to recovery during a primary virus infection.…”

Section: Discussionmentioning

confidence: 99%

“…A number of studies have demonstrated that immunosuppression may potentiate a primary virus infection and that this potentiation may be accompanied by a suppression of neutralizing antibody formation and by a more severe vireinia (17)(18)(19)(20)(21). In most of these studies it is likely that cellular immunity was also suppressed to some extent, and specific replacement with antibody or immune cells has generally not been performed.…”

Section: Discussionmentioning

confidence: 99%

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Mechanism of Recovery From Systemic Vaccinia Virus Infection

Worthington

Rabson

Baron

1972

The Journal of Experimental Medicine

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Administration of Cytoxan in doses capable of inhibiting both humoral and cellular immunity markedly potentiated primary systemic vaccinia virus infection in mice. Immunosuppressed mice did not form neutralizing antibody to vaccinia virus and had a prolonged and more severe viremia than nonimmunosuppressed control mice. Passive transfer of physiologic amounts of neutralizing antibody late in the course of infection, at a time when nonimmunosuppressed mice had similar levels of serum antibody, largely reversed the effect of Cytoxan on vaccinia virus infection. Transfer of 100 million immune spleen cells was much less effective than antibody in reversing the effect of Cytoxan on vaccinia virus infection, and mice receiving these cells did make some antibody. Serum interferon levels were not affected by Cytoxan. The results suggest an essential role for humoral antibody, but not for cellular immunity, in recovery from primary vaccinia virus infection in the mouse.

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Experimental Parainfluenza Type 1 Virus-Induced Encephalopathy in Adult Mice

Zgórniak-Nowosielska¹,

Iwasaki²,

Tachovsky³

et al. 1976

Arch Neurol

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The pathogenicity of the 6/94 strain of parainfluenza type 1 virus, originally isolated from multiple sclerosis brain, was studied in adult mouse brains. Intracerebral inoculation of the virus caused mononuclear cell infiltration in the form of perivascular cuffing and a diffuse exudation into the parenchymal tissue, preferentially in cerebral white matter, that resulted in marked degeneration over a 90-day observation period. Immunofluorescent staining revealed viral antigen in the ependymal lining cells only during the first seven days after infection. No correlation was found between the severity of the brain lesions and the level of circulating antiviral antibody, preexisting or newly produced.

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The Effect Of Cyclophosphamide On Sendai Virus Infection Of Mice

Cited by 41 publications

References 1 publication

Intestinal Resistance in the Experimental Enteric Infection of Mice with a Mouse Adenovirus

Intestinal Resistance in the Experimental Enteric Infection of Mice with a Mouse Adenovirus

Mechanism of Recovery From Systemic Vaccinia Virus Infection

Experimental Parainfluenza Type 1 Virus-Induced Encephalopathy in Adult Mice

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